A productive infection by vaccinia virus involves entry into the cell; expression and replication of the genome; defense against specific and non-specific host immune mechanisms; and assembly and release of infectious, enveloped, virus particles. Many of these steps involve interactions of viral proteins with cellular proteins or membranes. Combined genetic, biochemical, and electron microscopic approaches are being used to investigate these complex processes. During the past year, we made progress in understanding steps in the formation and transmission of extracellular virions. Evidence was obtained for the presence of a Golgi network retention signal within either the cytoplasmic or transmembrane domains of the B5R glycoprotein, which is required for Golgi membrane wrapping of intracellular mature virions. Other studies indicated that the glycoprotein encoded by the A34R gene is needed to form actin tails, which propel wrapped vaccinia virus particles, and to form specialized microvilli that spread vaccinia virus to neighboring uninfected cells.